Vasomotor Regulation of the Pulmonary Circulation

Three separate mechanisms could be responsible for contraction or dilata­ tion of pulmonary vessels: (a) the vagus and sympathetic nerves acting as the efferent limbs of reflex pathways, (b) humoral agents, such as the catecholamines, that are brought to the pulmonary vessels from afar via the blood stream, and (c) local effects that begin and end within the lungs (22). Under experimental conditions each of these is usually tested singly; under more natural circumstances they are apt to act in concert. Separate chapters in this volume deal extensively with the first two of these mechanisms (see chapters by Bergofsky and by Culver & Butler). This chapter focuses on the local effects. Four vasoregulatory systems known to be operative in the systemic circu­ lation have been sought in the pulmonary circulation: vasomotor critical closure of small muscular arteries, axon reflexes, reactive hyperemia, and baroreceptor reflexes. None of these could be shown to be involved in local vasomotor regulation in the lungs. On the other hand, the respiratory gases prove to be of paramount importance. A decrease in the oxygen tension of inspired gas proved remarkably effective in evoking pulmonary vasocon­ striction. Hypercapnia, which seems to act by producing acidosis locally (5, 66), was not quite as effective; somehow, however, it potentiated the hypoxic pressor response (33, 52). Alkalosis generally depressed the hypoxic response (63). A large literature points out the importance of this local control by respiratory gases in lung disease, where it constitutes an important mechanism for readjusting blood flow to well ventilated parts of the lungs (21, 33). Because of the wealth of experimental information about